Effect of tea polyphenols on growth of oral squamous carcinoma cells in vitro.

Epidemiologic evidence indicates that both black and green tea is a rich source of flavonoids and other polyphenolic antioxidants which protects against heart disease and cancer. In the current investigation, utilizing human oral squamous carcinoma cell line SCC-25, we have evaluated the effect of three major tea constituents, (-)-epigallocatechin-3-gallate (EGCG), (-)-epicatechin-3-gallate (ECG) and (-)-epigallocatechin (EGC) on cell growth and DNA synthesis. Test agents in concentrations of 50, 80, 100 and 200 microM were incubated in triplicates in DMEM-HAM's F-12 (50: 50) supplemented with 10% calf serum and antibiotics in an atmosphere of 5% CO2 in air for 72 hrs. Cell growth was determined by alamarBlue assay method and DNA synthesis was measured by the incorporation of [3H]-thymidine in nuclear DNA. At the four dose levels used, the three compounds induced significant dose-dependent inhibition in cell growth. In DNA study, the three compounds exhibited stimulatory effect at 50 microM followed by significant dose-dependent inhibitory effect (10 to 100%) at 80, 100 and 200 microM dose levels. Dose-dependent changes in cell morphology were also observed with phase-contrast microscopy after cell treatment with EGCG.

The inhibitory effect of curcumin, genistein, quercetin and cisplatin on the growth of oral cancer cells in vitro.

Epidemiological evidence indicates that plant derived flavonoids and other phenolic antioxidants protect against heart disease and cancer. In the current investigation utilizing human oral squamous carcinoma cell line (SCC-25), we have evaluated the potency of three different plant phenolics, viz., curcumin, genistein and quercetin in comparison with that of cisplatin on growth and proliferation of SCC-25. Test agents were dissolved in DMSO and incubated in triplicates in 25 cm2 flasks in DMEM- HAM's F-12 (50:50)supplemented with 10% calf serum and antibiotics in an atmosphere 5% CO2 in air for 72 hours cell growth was determined by counting the number of cells in a hemocytometer. Cell proliferation was determined by measuring DNA synthesis by the incorporation of [3H]-thymidine in nuclear DNA. Cisplatin (0.1, 1.0, 10.0 microM) and curcumin (0.1, 1.0, 10.0 microM) induced significant dose-dependent inhibition in both cell growth as well as cell proliferation. Genistein and quercetin (1.0, 10.0, 100.0 microM) had biphasic effect, depending on their concentrations, on cell growth as well as cell proliferation. Based on these findings, it is concluded that curcumin is considerably more potent than genistein and quercetin, but cisplatin is five fold more potent than curcumin in inhibition of growth and DNA synthesis in SCC-25.

Biphasic action of vitamin E on the growth of human oral squamous carcinoma cells.

Treatment of human tongue squamous carcinoma cell, SCC-25, with physiological concentrations of vitamin E succinate (VES) which varied from 0.001 to 50 mumoles/L resulted in significant dose-dependent stimulation of cell growth. Whereas, pharmacological doses of the vitamin (100-154 microM) induced significant inhibition in cell growth. The possible anticarcinogenic mechanisms of action of vitamin E are discussed.

Modulating effect of resveratrol and quercetin on oral cancer cell growth and proliferation.

Resveratrol and quercetin are polyphenols which have been detected in significant amounts in green vegetables, citrus fruits and red grape wines. Beneficial effects attributed to these compounds include anti-inflammatory, antiviral and antitumor properties. The effect of resveratrol and quercetin on growth of human oral cancer cells is unknown. Resveratrol and quercetin, in concentrations of 1 to 100 microM, were incubated in triplicates with human oral squamous carcinoma cells SCC-25 in DMEM-HAM's F-12 supplemented with fetal calf serum and antibiotics in an atmosphere of 5% CO2 in air at 37 degrees C for 72 h. Cell growth was determined by counting the number of viable cells with a hemocytometer. Cell proliferation was measured by means of incorporation of [3H]thymidine in nuclear DNA. Resveratrol at 10 and 100 microM induced significant dose-dependent inhibition in cell growth as well as in DNA synthesis. Quercetin exhibited a biphasic effect, stimulation at 1 and 10 microM, and minimal inhibition at 100 microM in cell growth and DNA synthesis. Combining 50 microM of resveratrol with 10, 25 and 50 microM of quercetin resulted in a gradual and significant increase in the inhibitory effect of quercetin on cell growth and DNA synthesis. We conclude that resveratrol or a combination of resveratrol and quercetin, in concentrations equivalent to that present in red wines, are effective inhibitors of oral squamous carcinoma cell (SCC-25) growth and proliferation, and warrant further investigation as cancer chemopreventive agents.

The effect of red wine and its components on growth and proliferation of human oral squamous carcinoma cells.

Epidemiologic evidence indicates that red wine may contain phenolic compounds which protect against heart disease and cancer. Resveratrol and quercetin are wine phenolics which possess antioxidant and antimutagenic effects. Resveratrol at 10 and 100 microM induced significant dose-dependent inhibition in human oral squamous carcinoma cell (SCC-25) growth and DNA synthesis. Quercetin exhibited a biphasic effect, stimulation at 1.0 and 10 microM and minimal inhibition at 100 microM in cell growth and DNA synthesis. Combining 50 microM of resveratrol with 10, 25 and 50 microM of quercetin resulted in gradual and significant increase in the inhibitory effect of the two compounds. Diluted red wine which contained only 1.6 microM of each of resveratrol and quercetin had significantly more inhibitory effect on cell growth, DNA synthesis and changes in cell morphology than each compound alone or in combination. We conclude that: (i) Resveratrol by itself or a combination of resveratrol and quercetin are effective inhibitors of SCC-25 growth and DNA synthesis. (ii) The presence of other wine phenolic phytochemicals enhance significantly the effect of resveratrol and quercetin on inhibition of cancer cell growth and DNA synthesis.

Inhibition of growth in oral squamous carcinoma cells by cyclopentenone prostaglandins: comparison with chemotherapeutic agents.

Four cyclopentenone prostaglandins (CPPGs) and PGE2 caused significant dose-dependent inhibition in growth of human oral squamous carcinoma cells (SCC-15). The rank order of their potency was PGJ2>PGA1>16, 16-dimethyl PGA1>PGA2>PGE2. In a follow-up experiment it was found that the mean per cent inhibition in cell growth by PGJ2 and delta12-PGJ2 at 10(-5) M was 61.22 and 63.81, while that of 5-fluorouracil and methotrexate was 36.67 and 38.86, respectively. delta12-PGJ2 and PGJ2 induced significant dose-dependent inhibition in nuclear DNA synthesis (i.e. cell proliferation). Combining vitamin E succinate with lower concentrations of CPPGs enhanced significantly their inhibitory effect on nuclear DNA synthesis of cancer cells.

Effects of indomethacin, cisplatin and delta 12-prostaglandin J2 on growth of oral squamous carcinoma cells.

The effect of indomethacin, cisplatin and delta 12-prostaglandin J2 (PGJ2) on the inhibition of cell growth and DNA Synthesis (i.e. cell proliferation), was evaluated in vitro on human oral squamous carcinoma cells(SCC-25). The rank order of their inhibitory potency at 10(-5) M was delta 12-PGJ2 > cisplatin > indomethacin. However, delta 12-PGJ2 at 10(-7) and 10(-6) M induced a significant stimulatory effect on cell growth as well as DNA synthesis. The sefindings suggest that delta 12-PGJ2 is a promising novel chemotherapeutic agent for oral cancer and potential candidate for future clinical investigations.

Erroneously low results due to high nonspecific binding encountered with a radioassay kit that measures true serum vitamin B12.

Subsequent to recent disclosures that low serum vitamin B12 results can appear normal using many of the current radioassay methods because of the presence of cobalamin (vitamin B12) analogues in human serum, a number of radioassay kits have become available with modified intrinsic factor preparations and claims of measuring "true" vitamin B12. While evaluating two of these kits, one with R protein activity blocked and the other with R protein removed, the possibility was discovered that normal results could appear low owing to high nonspecific binding encountered with one of the methodologies. The problem of nonspecific binding was apparently due to incomplete inactivation of serum endogenous binding proteins and inadequate separation of free and bound radioisotope. The results demonstrate that "lower" vitamin B12 values are not necessarily "truer" values, and therefore caution and critical evaluation should temper the haste to change to commercial radioassay procedures that claim to provide "true" vitamin B12 levels.